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SYN3 is a member of the synapsin gene family. Additionally we are shipping Synapsin III Antibodies (32) and Synapsin III Proteins (5) and many more products for this protein.
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This study demonstrated that synapsin 3 regulating GABA Release from Hippocampal Interneurons.
These findings support a reciprocal modulatory interaction of alpha-syn and synapsin III in the regulation of dopamine neuron synaptic function.
Behavioral and neurophysiological features of Syn3 knockout mice are characterized by observation of the development and progress of seizures from postnatal day 20 to 180.
Analysis of cultured neurons from wild-type and Syn (show SYP ELISA Kits) I,II,III-deficient triple knock-out (TKO (show MRPS12 ELISA Kits)) mice shows that synaptic vesicles are severely dispersed in the absence of Syns.
Mice lacking synapsin III show abnormalities in explicit memory and conditioned fear
Collectively, our results demonstrate a novel role for synapsin III in regulating the proliferation of neural progenitor cells in the adult hippocampal dentate gyrus.
These findings contribute to previous work showing dysregulation of Synapsins, particularly SYN2 (show SYN2 ELISA Kits), in mood disorders and improve our understanding of the regulatory mechanisms that precipitate these changes likely leading to the BD or MDD phenotype.
Syn-3 may mimic Syn (show FYN ELISA Kits)-1A in the ability to bind and modulate Cavs, but preferring Cav2.3 (show CACNA1E ELISA Kits) to perhaps participate in triggering fusion of newcomer insulin (show INS ELISA Kits) SGs (show FBN1 ELISA Kits) during second-phase GSIS.
The variations of MnSOD (show SOD2 ELISA Kits) (rs4880) and SYN (show FYN ELISA Kits) III (rs3788470, rs3827336, rs5998557) were not major risk factors for PD among Chinese, at least in our study populations
A significant difference was determined between attention deficit hyperactivity disorder and synapsin III gene -631 C>G polymorphism compared to the control group.
Evidence is not in favor of a large effect of synapsin III gene in the pathogenesis of schizophrenia.
A missense polymorphism, S470N, was identified in the synapsin III gene and appeared more frequently in individuals with schizophrenia. The site affected by the polymorphism, Ser470, was determined to be a substrate for mitogen-activated protein kinase (show MAPK1 ELISA Kits).
Supports a role for synapsin III in a subset of African American patients with schizophrenia.
A trend towards significance was detected when the synapsin III -196A allele distribution was analyzed in Caucasian patients with schizophrenia and a cohort of subjects from the Czech Republic with bipolar disorder.
No evidence that the synapsin III locus as a major susceptibility locus contributing to attention deficit hyperactivity disorder.
This gene is a member of the synapsin gene family. Synapsins encode neuronal phosphoproteins which associate with the cytoplasmic surface of synaptic vesicles. Family members are characterized by common protein domains, and they are implicated in synaptogenesis and the modulation of neurotransmitter release, suggesting a potential role in several neuropsychiatric diseases. The protein encoded by this gene shares the synapsin family domain model, with domains A, C, and E exhibiting the highest degree of conservation. The protein contains a unique domain J, located between domains C and E. Based on this gene's localization to 22q12.3, a possible schizophrenia susceptibility locus, and the established neurobiological roles of the synapsins, this family member may represent a candidate gene for schizophrenia. The TIMP3 gene is located within an intron of this gene and is transcribed in the opposite direction. Alternative splicing of this gene results in multiple splice variants that encode different isoforms.
, synapsin 3a
, synapsin III isoform IIIa
, synapsin 3
, synapsin IIIa
, cN28H9.2 (synapsin III)